Source of Free Radicals and Consequences of Oxidative Stress Following Secondary Brain Injury after Intracerebral Haemorrhage

Free radicals are reactive chemical species having a single unpaired electron in an outer orbit. Intracranial haemorrhage (ICH) is an acute and spontaneous extravasation of blood into the cranial vault. The most important sites of ICH are basal ganglia followed by cerebral hemispheres. The pathological mechanisms of hematoma after ICH within brain parenchyma trigger a series of adverse events causing secondary brain injury and severe neurological deficits. The global incidence of ICH is increasing year by year, with a trend towards growing incidence at a younger age. A variety of pathways can induce the generation of free radicals in secondary brain injury after ICH. During ICH, mitochondria dysfunction occurs, and substantial ROS production follows. Iron overload is also involved in secondary brain injury, leading to neuronal death, brain edema, and neurodeficits after ICH. Neuroinflammation is recognized as a vital factor in the pathophysiology of ICH-induced brain injury. After ICH, both oxidative and ER stress levels are upregulated and NADPH oxidase is thought to play an important contact role during the oxidative and ER stress process. Excessive free radicals can cause the peroxidation of lipid, protein, and nucleic acid through direct and indirect pathways, leading to apoptosis. Autophagy may also play different roles in pathogenesis at different stages of cerebral hemorrhage. Electronic search was carried out through the period up to 2020.

Keywords:Free radicals; Oxidative stress; Intracerebral haemorrhage; Secondary brain injury after intracerebral haemorrhage